Evidence map›Paper›PMID 25642299›Full record

ArticleJournal of arrhythmia2014

Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.

Norishige Morita, William J Mandel, Yoshinori Kobayashi, Hrayr S Karagueuzian

Open access · goldAbstract read
In one paragraph

Article in Journal of arrhythmia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Dose- and genotype-dependent cardiac arrhythmia and sudden death in rats following microdystrophin gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  10. Article
  11. Patient Outcomes by Ventricular Systolic and Diastolic Function.Journal of the American Heart Association · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Norishige MoritaDivision of Cardiology, Department of Medicine, Tokai University Hachioji Hospital, Tokyo, Japan.
William J MandelTranslational Arrhythmia Research Section, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California.
Yoshinori KobayashiDivision of Cardiology, Department of Medicine, Tokai University Hachioji Hospital, Tokyo, Japan.
Hrayr S KaragueuzianDivision of Cardiology, Department of Medicine, Tokai University Hachioji Hospital, Tokyo, Japan.
Tokai University Hachioji Hospital · JPUCLA Health · USUniversity of California, Los Angeles · US

Funding

WAVE DYNAMICS IN NORMAL AND DISEASED RABBIT HEARTSP01HL078931 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHEN, PENG-SHENG · 2005 to 2015
$20.7M
NHLBI NIH HHS P01 HL078931
6 · The paper itself

Abstract

Animal and emerging clinical studies have demonstrated that increased ventricular fibrosis in a setting of reduced repolarization reserve promotes early afterdepolarizations (EADs) and triggered activity that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF). Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative and metabolic stress-induced EADs to manifest as triggered activity causing VT/VF. The lack of such an arrhythmogenic effect by the same stressors in normal non-fibrotic hearts highlights the importance of fibrosis in the initiation of VT/VF. These findings suggest that antifibrotic therapy combined with therapy designed to increase ventricular repolarization reserve may act synergistically to reduce the risk of sudden cardiac death.

Indexed as

anti-fibrotic therapyCardiac fibrosisoxidative stressrepolarization reserveventricular fibrillation

Identifiers

PMID25642299
PMCPMC4308294
OpenAlexW2072260252

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.